Aims: This study aimed to investigate their vasorelaxation potential and the possible involvement of autonomic receptors and nitric oxide in mediating their effect.

Settings and Design: Both extracts will be tested on isolated thoracic aorta rings of WKY and SHR. The involvement of autonomic receptors and nitric oxide will be elucidated using respective blockers.

Materials and Methods: Isolated thoracic aorta rings from WKY and SHR were mounted onto myograph chambers to measure changes in the aorta tension. Increasing concentrations of AESP and MESP, from 1 μg/ml to 10 mg/ml were added onto the myograph chambers. Blockers such as atropine (1 μM), phentolamine (1 μM), propranolol (1 μM), and Nω-nitro-l-arginine methyl ester (100 μM) were preincubated before addition of extracts to check for involvement of muscarinic, α- and β-adrenergic receptors (AR) as well as nitric oxide, respectively.

Statistical Analysis Used: Two-way ANOVA, followed by post hoc Bonferroni test was used, where P < 0.05 (two-tailed) was considered statistically significant.

Results: AESP and MESP caused significant vasorelaxations through nitric oxide pathway. The former was mediated through α-AR while the latter was mediated by β-adrenergic and muscarinic receptors.

Conclusion: Vasorelaxation effect by AESP and MESP involved nitric oxide pathway which is possibly mediated by the autonomic receptors.

METHODS: Thirty healthy Muslim men participated in the study. Their electrocardiograms and EEGs were continuously recorded before, during, and after salat practice with a computer-based data acquisition system (MP150, BIOPAC Systems Inc., Camino Goleta, California). Power spectral analysis was conducted to extract the RPα and HRV components.

METHODS: We adopted a nested case-control design within a cohort of school teachers. Working teachers from six states of Peninsular Malaysia, and had experienced incident CVD before a right-censored date (31st December 2021) were defined as cases. Incident CVD was operationally defined as the development of non-fatal acute coronary syndrome (ACS), stroke, congestive cardiac failure, deep vein thrombosis or peripheral arterial disease before the censored date. Controls were working teachers who did not acquire an incident CVD before the similar right-censored date. All controls were randomly selected, with a ratio of one case to four controls, from among the working teachers in one of the states in Peninsular Malaysia. We used a shortened version of the Malay-validated World Health Organization-Health and Work Performance Questionnaire (WHO-HPQ) to estimate the workplace productivity effect among teachers with incident CVD (cases). The same questionnaire was distributed to teachers in a single state of Peninsular Malaysia who did not experience incident CVD (controls). Absenteeism, presenteeism and annual monetary loss were computed based on the scoring rules in the WHO-HPQ. Analysis of covariance was performed with covariate adjustment using propensity scores. The bootstrapping method was applied to obtain better estimates of marginal mean differences, along with standard errors (SE) and appropriate effect sizes.

METHODS: A panel comprising cardiologists from China, Hong Kong, India, Japan, Malaysia, Pakistan, Philippines, Singapore, South Korea, Taiwan, and Thailand convened to share insights and provide guidance for the optimal management of iron deficiency in patients with HF, tailored for the Asian community.

RESULTS: Expert opinions were provided for the screening, diagnosis, treatment and monitoring of iron deficiency in patients with HF. It was recommended that all patients with HF with reduced ejection fraction should be screened for iron deficiency, and iron-deficient patients should be treated with intravenous iron. Monitoring of iron levels in patients with HF should be carried out once or twice yearly. Barriers to the management of iron deficiency in patients with HF in the region include low awareness of iron deficiency amongst general physicians, lack of reimbursement for screening and treatment, and lack of proper facilities for administration of intravenous iron.

AIM: To investigate the effect of SBH administration on the kidney and liver of streptozotocin-induced (STZ; 55 mg/kg) diabetic Sprague Dawley rats.

METHODS: The rats were grouped as follows (n = 6 per group): non-diabetic (ND), untreated diabetic (UNT), metformin-treated (MET), and SBH+metformin-treated (SBME) groups. After successful diabetic induction, ND and UNT rats were given normal saline, whereas the treatment groups received SBH (2.0 g/kg and/or metformin (250 mg/kg) for 12 d. Serum biochemical parameters and histological changes using hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining were evaluated.

RESULTS: On H&E and PAS staining, the ND group showed normal architecture and cellularity of Bowman's capsule and tubules, whereas the UNT and MET groups had an increased glomerular cellularity and thickened basement membrane. The SBH-treated group showed a decrease in hydropic changes and mild cellularity of the glomerulus vs the ND group based on H&E staining, but the two were similar on PAS staining. Likewise, the SBME-treated group had an increase in cellularity of the glomerulus on H&E staining, but it was comparable to the SBH and ND groups on PAS staining. UNT diabetic rats had tubular hydropic tubules, which were smaller than other groups. Reduced fatty vacuole formation and dilated blood sinusoids in liver tissue were seen in the SBH group. Conversely, the UNT group had high glucose levels, which subsequently increased MDA levels, ultimately leading to liver damage. SBH treatment reduced this damage, as evidenced by having the lowest fasting glucose, serum alanine transaminase, aspartate transaminase, and alkaline phosphatase levels compared to other groups, although the levels of liver enzymes were not statistically significant.